Transient receptor potential vanilloid type 1 (TRPV1)is highly expressed in cardiac sensory neurons and has a crucial role in detecting myocardial ischemia.
The equilibrative nucleoside transporter-1 (ENT1, SLC29A1) is an important drug target, as transporter inhibition is a potential treatment of ischemic heart disease, stroke, and cancer.
We also provide a comprehensive review of the current state of knowledge concerning the role of high factor VIII levels in determining the risk of arterial thrombosis or ischemic heart disease (IHD).
Hypoxia-inducible factors are stabilized and provide protection from ischemia and reperfusion injury in the setting of myocardial ischemia.In the setting of ischemia, myocyte-specific hypoxia-inducible factor 2A induces expression of amphiregulin, which is an epidermal growth factor that binds to epidermal growth factor receptor 1 (ERBB1) in the myocardium.
These findings suggest that hypoxia-inducible factor 2A promotes transcription-independent induction of ERBB1 protein and implicates epidermal growth factor signaling in protection from myocardial ischemia and reperfusion injury.
Myocyte-specific Hif2a or ErbB1 knockout mice were generated to observe the effect of Hif2a knockdown in regulating ERBB1 expression and to examine the role of ERBB1 during myocardial ischemia and reperfusion injury.
Myocyte-specific Hif2a or ErbB1 knockout mice were generated to observe the effect of Hif2a knockdown in regulating ERBB1 expression and to examine the role of ERBB1 during myocardial ischemia and reperfusion injury.
Our results showed that miR-206 inhibitor alleviated ischemia-reperfusion-induced arrhythmias, indicated by the lower extent of changes in heart rate (HR), PR interval, rate pressure product (RPP), and mean arterial pressure (MAP). miR-206 inhibitor also downregulated the serum creatine kinase isoenzyme (CKMB) and cardiac troponin I (cTnI) levels in mice under myocardial ischemia-reperfusion (IR) process.
Our results showed that miR-206 inhibitor alleviated ischemia-reperfusion-induced arrhythmias, indicated by the lower extent of changes in heart rate (HR), PR interval, rate pressure product (RPP), and mean arterial pressure (MAP). miR-206 inhibitor also downregulated the serum creatine kinase isoenzyme (CKMB) and cardiac troponin I (cTnI) levels in mice under myocardial ischemia-reperfusion (IR) process.
Vildagliptin and sitagliptin are anti-diabetic drugs of the dipeptidyl peptidase-4 (DPP-4) inhibitors that have a protective role against cerebral ischemic stroke and cardiac ischemia reperfusion.
NSTEMI patients without chest pain were significantly older, had lower SBP, more tachycardia, more cerebrovascular disease, but less ischemic heart disease.
NSTEMI patients without chest pain were significantly older, had lower SBP, more tachycardia, more cerebrovascular disease, but less ischemic heart disease.
NSTEMI patients without chest pain were significantly older, had lower SBP, more tachycardia, more cerebrovascular disease, but less ischemic heart disease.
That this has resulted in lower blood levels of IP-TFA in the United States is clear, but whether this has been accompanied by a reduction in the incidence of fatal IHD is unknown.
These observations suggest that PCSK9 is inter-twined with inflammation with implications in atherosclerosis and its major consequence - myocardial ischemia.
Other possible mechanisms include inhibition of sodium-hydrogen exchange, increases in erythropoietin levels, and reduction in myocardial ischemia or reperfusion injury.